PMID- 24391982
OWN - NLM
STAT- MEDLINE
DCOM- 20140902
LR  - 20220311
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 12
DP  - 2013
TI  - Dickkopf-1 is oncogenic and involved in invasive growth in non small cell lung 
      cancer.
PG  - e84944
LID - 10.1371/journal.pone.0084944 [doi]
LID - e84944
AB  - Dickkopf-1 (DKK1) is an inhibitor of the Wnt/beta-catenin signaling pathway. 
      However, the role of DKK1 in the progression of non small cell lung cancer 
      (NSCLC) is not fully understood. In this study, RT-PCR and Western blot were used 
      to examine the expression of DKK1 in a panel of ten human NSCLC cell lines and 
      NSCLC tissues. DKK1 expression was highly transactivated in the great majority of 
      these cancer lines. The expression of DKK1 was upregulated on both mRNA and 
      protein levels in NSCLC tissues compared with the adjacent normal lung tissues. 
      Immunohistochemistry and immunofluoresence revealed that DKK1 was mainly 
      distributed in the cytoplasm in both carcinoma tissues and cell lines. DKK1 
      protein expression was also evaluated in paraffin sections from 102 patients with 
      NSCLC by immunohistochemistry, and 65(63.73%)tumors were DKK1 positive. Relative 
      analysis showed a significant relationship between DKK1 positive expression and 
      lymph node metastasis(P<0.05). Patients with DKK1-positive tumors had poorer DFS 
      than those with negative ESCC (5-year DFS; 15.4% versus 27%, P = 0.007). To 
      further explore the biological effects of DKK1 in NSCLC cells, we over-expressed 
      DKK1 in NSCLC 95C cell using eukaryotic expression vector pCMV-Tab-2b and 
      performed a knockdown of DKK1 in LTEP-a-2 cell using a short hairpin RNA 
      expression vector pSilencer 5.1. DKK1 did not have any effect on proliferation, 
      but seemed to play a role in migration and invasion capability. Overexpression of 
      DKK1 promotes migratory and invasive activity of 95C, while DKK1 knockdown 
      resulted in the suppression of migration and invasion potentials of LTEP-a-2 
      cell. Taken together, these results indicate that DKK1 may be a crucial regulator 
      in the progression of NSCLC. DKK1 might be a potential therapeutic target in 
      NSCLC.
FAU - Li, Shujun
AU  - Li S
AD  - The Second Hospital of Hebei Medical University, Shijiazhuang, China.
FAU - Qin, Xuebo
AU  - Qin X
AD  - Hebei Chest Hospital, Shijiazhuang, China.
FAU - Guo, Xin
AU  - Guo X
AD  - The Second Hospital of Hebei Medical University, Shijiazhuang, China.
FAU - Cui, Airong
AU  - Cui A
AD  - The Second Hospital of Hebei Medical University, Shijiazhuang, China.
FAU - He, Yuzheng
AU  - He Y
AD  - The Second Hospital of Hebei Medical University, Shijiazhuang, China.
FAU - Wei, Sen
AU  - Wei S
AD  - Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, 
      Tianjin, China.
FAU - Wang, Xiaolu
AU  - Wang X
AD  - The Second Hospital of Hebei Medical University, Shijiazhuang, China.
FAU - Shan, Baoen
AU  - Shan B
AD  - The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
LA  - eng
PT  - Journal Article
DEP - 20131231
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (DKK1 protein, human)
RN  - 0 (DNA Primers)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
SB  - IM
MH  - Blotting, Western
MH  - Carcinoma, Non-Small-Cell Lung/*genetics
MH  - Cell Line, Tumor
MH  - DNA Primers/genetics
MH  - Fluorescent Antibody Technique
MH  - Gene Expression Regulation, Neoplastic/genetics/*physiology
MH  - Genetic Vectors
MH  - Humans
MH  - Immunohistochemistry
MH  - Intercellular Signaling Peptides and Proteins/genetics/*metabolism
MH  - Kaplan-Meier Estimate
MH  - Lymphatic Metastasis/*genetics
MH  - Neoplasm Invasiveness/*genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
PMC - PMC3877398
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2014/01/07 06:00
MHDA- 2014/09/03 06:00
PMCR- 2013/12/31
CRDT- 2014/01/07 06:00
PHST- 2013/04/26 00:00 [received]
PHST- 2013/11/19 00:00 [accepted]
PHST- 2014/01/07 06:00 [entrez]
PHST- 2014/01/07 06:00 [pubmed]
PHST- 2014/09/03 06:00 [medline]
PHST- 2013/12/31 00:00 [pmc-release]
AID - PONE-D-13-17398 [pii]
AID - 10.1371/journal.pone.0084944 [doi]
PST - epublish
SO  - PLoS One. 2013 Dec 31;8(12):e84944. doi: 10.1371/journal.pone.0084944. 
      eCollection 2013.